Abstract
Background: Mannose-binding lectin (MBL) is a pattern-recognition molecule of the innate immune system and may be involved in the pathogenesis of inflammatory bowel disease (IBD). Our aim was to assess the prevalence of MBL deficiency in a cohort of patients with paediatric-onset IBD and study whether it is associated with the clinical manifestations, serum antibody formation, or genetic factors. Methods: This prospective study included 159 paediatric patients (mean age: 14.0. years) with IBD [107 patients with Crohn disease (CD) and 52 patients with ulcerative colitis (UC)]. Furthermore, 95 controls were investigated. Serum samples were determined for MBL by enzyme-linked immunosorbent assay (ELISA) and for serologic markers [autoantibodies against Saccharomyces cerevisiae (ASCA) and perinuclear components of neutrophils (pANCA)] by indirect immunofluorescent assay. NOD2/CARD15 variants were tested by polymerase chain reaction/restriction fragment length polymorphism. Results: The MBL serum concentration was significantly lower in IBD patients(both with CD and UC) compared to controls (IBD, p = 0.007, CD, p = 0.04, UC p = 0.004). Prevalence of low MBL level (< 500. ng/mL) was significantly higher in both CD and UC groups compared to controls (p = 0.002 and p = 0.006). Furthermore, low MBL level was associated with isolated ileal involvement (p = 0.01) and MBL deficiency (< 100. ng/mL) with male gender (p = 0.004) in patients with CD. We failed to confirm any correlation between MBL deficiency and serum autoantibodies or NOD2/CARD15 variants. Conclusions: Our results suggest that low MBL associated with paediatric-onset IBD and ileal CD may be considered an additional marker of the IBD pathogenesis. © 2012 European Crohn's and Colitis Organisation.
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Kovacs, M., Papp, M., Lakatos, P. L., Jacobsen, S., Nemes, E., Polgar, M., … Veres, G. (2013). Low mannose-binding lectin (MBL) is associated with paediatric inflammatory bowel diseases and ileal involvement in patients with Crohn disease. Journal of Crohn’s and Colitis, 7(2), 134–141. https://doi.org/10.1016/j.crohns.2012.03.008
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